Answer is A. 18%, 2nd degree deep partial thickness

Discussion
Burns are fairly common, accounting for the 4th leading cause of trauma worldwide3. There is an increased prevalence of burns in lower socioeconomic populations and most burns occur in the home3. The three major causes of burns are by heat including flame or scalding liquid, chemicals, or electricity.
Burns are categorized by the depth of skin and tissue evolvement. Traditionally, burns were divided into four categories 1st, 2nd, 3rd, and 4th degree burns. Today, we have transitioned into categorizing based on thickness; superficial, partial thickness, and full thickness2. Superficial is defined as affecting only the epidermis, appearing red, easily blanchable and patients have mild to moderate pain. Partial thickness can be further broken into superficial and deep. Superficial partial thickness involves the entire epidermis and only the superficial dermis. These burns appear erythematous, moist, with blisters, and patients usually have severe pain. Deep partial thickness involves the epidermis and most of the dermis with some skin appendages destroyed. These burns present as white and erythematous areas, dry, waxy and decreased blanching to pressure. In certain areas, usually where the skin appears white, their pain will be decreased. Lastly, full thickness burns affect all layers where the appendages are completely destroyed. Patients will present with white, charred skin that are dry and leathery and are not blanchable. These patient will usually be without pain4.
It is important to obtain a full history and physical from this patient population, specifically the cause and length of exposure, degree of pain, and any other medical conditions that may worsen the prognosis or change the treatment3. If the burn was caused by fire, it is crucial to assess for symptoms of smoke inhalation. Symptoms include shortness of breath, sore throat, soot around the nares, or singed facial hair3. It is important to assess the depth of burn as described above and estimate the total area of the burn3. The rules of nine is a universal tool to calculate total body surface area and further assisting in the treatment plans for burns. The body is divided in multiples of 9, each arm 9% (4.5% front and 4.5% back), the head both front and back totaling 9%, Front of the torso 18% (upper 9%, lower 9%), Back 18%, each leg 18% (front 9%, back 9%), and genitalia 1%4.
Diagnostics studies are dependent on the mechanism and duration of exposure. One should obtain a chest x-ray if there is question of smoke inhalation as well as carboxyhemoglobin levels and ABGs3. If the burn is of electric nature an EKG and CK levels are important to rule out any cardiovascular injury. Baseline labs are also an important tool to monitor and compare throughout the treatment process3.
The treatment of burns is very complex and dependent on the depth and total body surface area affected. Fluid resuscitation is crucial in these patients so much so a formula was created for specifically for burn treatment. The Parkland formula is an equation to calculate the total fluid requirements for a 24-hour period. Parkland Formula: 4ml x total body surface area % x body weight (kg). Once calculated, 50% of this total is given within the first eight hours and the rest is given in the remaining 16 hours4.
Another important aspect in managing these patient is pain control. Patients present in severe pain and require extensive and rapid pain relief. Fentanyl or Morphine are the analgesic drugs of choice for burn treatment3. Wound management is dependent on burn depth. All burns should be thoroughly cleaned with large amounts of water1. Superficial and superficial partial thickness burns heal quickly with wet dressings, silver sulfadiazine antibiotic cream or xeroform wound dressing1, 2. For deep partial thickness and full thickness burns, surgical intervention is usually necessary for treatment as these patients most likely require skin grafting1.

References

1.Centers WC. Partial thickness burns. Partial Thickness Burns. http://www.woundcarecenters.org/article/wound-types/partial-thickness-burns. Accessed July 12, 2017.
2.Davidge K. Older Adults and Burns. Medscape. http://www.medscape.com/viewarticle/579832_3. Accessed July 12, 2017.
3.DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 902902, Burns – emergency management; [updated 2017 Jun 22, cited place cited date here]; [about 4 screens]. Available from http://www.dynamed.com/login.aspx?direct=true&site=DynaMed&id=902902. Registration and login required.

4. Grabb W, Smith JW, Thorne CH, Chung KC, Gosain A. Grabb and Smiths plastic surgery. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2014

Correct Answer: E. Plasma Cells. Multiple Myeloma is a plasma cell dyscrasia which involves abnormal proliferation of a monoclonal population of plasma cells that commonly secrete high levels of monoclonal immunoglobulins (mostly IgG or IgA). Classic presentation of MM involves the acronym CRAB (high Calcium, Renal dysfunction, Anemia and Bone lytic lesions). Bone Marrow biopsy reveals >10% plasma cells. Options 1. NK cells, 2. Neutrophils, 3. T-lymphocytes are not associated with MM. Option 4. B-lymphocytes; Plasma cells are derived from B-lymphocytes. However, B-lymphocyte counts are not elevated in the Bone Marrow evaluation.
Discussion
Epidemiology: Multiple Myeloma (MM) is a plasma cell disorder where there is an abnormal proliferation of monoclonal population of plasma cells that secrete monoclonal immunoglobulins. It is the second most common hematological malignancy in US. It is a disease of an older population (median age of onset is 69 years). It affects men slightly more common than women and African Americans have twice the incidence and mortality as Caucasians.
Etiology: MM is a malignancy of terminally differentiated B-lymphocytes; the Plasma Cells, that is not completely understood. Some of the known predisposing factors includes ionizing radiation, environmental exposures (pesticides, herbicides and occupational exposures), MGUS, hereditary and viruses (increased risk in HIV).
Pathophysiology: A proposed model of disease progression: normal plasma cell->monoclonal gammopathy of undetermined significance (MGUS) ->MM. The major mutations associated with poor prognosis includes deletion (chromosome 13) and translocation (4; 14). Translocation (14;16) has conflicting data vs translocation (11;14) is associated with improved survival. The overall progression of MGUS toward plasma cell malignancy is at the rate of 1% per year with cumulative probability of 12 % at 10 years. Cytokines like Interleukin-6 (IL-6) is a growth factor secreted by MM cells that promotes its survival. It also secretes IL- 1 and soluble IL-6 receptor that activates osteoclast promoting bone resorption. Basic fibroblast growth factors (bFGF) and vascular endothelia growth factors (VEGF) are potent and synergistic mediators of angiogenesis that are elevated in MM and are used as markers for plasma Cell labeling index (PCLI) for evaluation of proliferative capacity of MM cells.
Historical and physical finding: Major symptoms of MM can be remembered by acronym CRAB. HyperCalcemia (Ca of >11.5) is a presenting feature in 30 % of the patients. Renal Dysfunction (Serum Creatinine of > 1.5) seen in up to 31 % of the cases and is primarily associated with tubular damage by monoclonal light chain protein. Anemia (Hgb Diagnostic Labs/Imagings: Common workup for MM includes CBC with differential, calcium, serum creatinine, LDH, albumin, β₂ macroglobulin, Bone Marrow Aspiration with cytogenetics and PCLI, chromosomal analysis with FISH, 24 urine for protein and UPEP with immunofixation, SPEP with immunofixation, Kappa and Lambda light chains and Skeletal survey.
Management/Treatment: Despite recent advances in treatment options, MM remains incurable. Goal of therapy remains disease control, improve quality of life and prolong survival. High dose chemotherapy followed by autologous Hematopoietic Stem cell Transplant remains the treatment of choice. Factors such as initial response to therapy, age, performance status, comorbidities, renal and pulmonary functions and active infection status defines their eligibility and success to transplant.
The patient had a classic presentation of symptomatic Myeloma with elevated monoclonal proteins in both urine and serum. His bone marrow biopsy at the time of initial diagnosis revealed 80 % plasma cells with plasmacytoma in the bones. Also, he had positive findings for renal impairment, anemia, bone involvement and recurrent infections.
References
1.Clinical features, laboratory manifestations, and diagnosis of multiple myeloma. https://www.uptodate.com/contents/clinical-features-laboratory-manifestations-and-diagnosis-of-multiple-myeloma?source=search_result&search=multiple myeloma&selectedTitle=1~150#H28. Accessed July 10, 2017.
2. Anderson KC. Multiple Myeloma: A Clinical Overview. Cancer Network . November 2011:1-8. file:///C:/Users/mamta/Downloads/Cancer_Network_-_Multiple_Myeloma_A_Clinical_Overview_-_2017-05-11.pdf. Accessed July 7, 2017.
3. Multiple myeloma. HomePage. https://bethematch.org/for-patients-and-families/learning-about-your-disease/multiple-myeloma/. Accessed July 10, 2017.
4. What Is Multiple Myeloma? American Cancer Society. https://www.cancer.org/cancer/multiple-myeloma/about/what-is-multiple-myeloma.
5. Guidelines. International Myeloma Working Group. http://imwg.myeloma.org/category/guidelines-2/. Accessed July 10, 2017. html. Accessed July 10, 2017.

Pyloric stenosis is diagnosed in around 1-8 out of every 1,000 births, with a 4-5:1 male to female ratio. The average age at diagnosis is 43.1 days1. It has been found, however, that a later age of diagnosis is associated with a greater degree of prematurity2. The delayed diagnosis in premature infants is due to low birth weight and an atypical presentation3. Pyloric stenosis is more common in white infants than those of Hispanic, black, or Asian descent3. The cause is unknown; however there have been some documented risk factors including male gender, prematurity, positive family history, and early use of erythromycin4.
Pyloric stenosis occurs when both the circular and longitudinal muscle layers of the pylorus become hypertrophic and hyperplastic. This causes a narrowing of the pyloric lumen and an inability for liquid to pass through. Although the cause is multifactorial, it is known to involve deficiency in neurons containing nitric oxide synthase, abnormal innervation of the myenteric plexus, and lack of exposure to vasoactive intestinal peptide (VIP)3. Nitric oxide synthase contributes to the relaxation of the smooth muscle in the myenteric plexus. VIP also contributes to relaxation of the stomach and can be found in breast milk. This could explain why formula-fed babies are more likely to develop pyloric stenosis3.
A classic presentation of pyloric stenosis involves non-bilious, post-prandial projectile vomiting between 2 and 6 weeks of age. Following emesis, the infant will typically be hungry immediately and want to be fed. It is common to see a distended upper abdomen after feeding accompanied by prominent peristaltic waves traveling from left to right. In a small percentage of patients, there is a palpable “olive” shaped mass in the right upper abdomen, representing the thickening of the pylorus muscle1.
Common lab findings include hypochloremic alkalosis and hypokalemia. Dehydration occurs in cases of advanced disease, which is reflected in elevated hemoglobin and hematocrit values1 or hyper/hyponatremia3. If the classic “olive” mass is not palpated, imaging studies can be used to arrive at a diagnosis. The first line imaging study for pyloric stenosis is an abdominal ultrasound. Positive findings include a hypoechoic muscle ring greater than 4mm thick and a pylorus length greater than 15mm1. If the US is unclear, a barium upper GI series may be performed. This would show retained contrast in the stomach and a long narrow channel with a double track of barium1.
First line treatment is a Ramstedt pyloromyotomy, which is typically performed laparoscopically. In this procedure, the outer layer of the pylorus is incised which allows the inner lining to bulge out, allowing gastric contents to pass through the lumen4. Before an infant is brought in for surgery, they will be made NPO and be given intravenous fluids and electrolytes to correct the deficiencies sustained from vomiting3. If for some reason general anesthesia is contraindicated, the infant can be treated non-surgically with atropine sulfate, however this route has a lower success rate than a pyloromyotomy3.
The answer to the self-assessment question is B, female gender. As stated above, pyloric stenosis is most common in males with around a 4-5:1 predominance. Caucasian infants are 25% more likely to develop pyloric stenosis than Hispanics, and almost 75% more likely than blacks or Asians3. Pyloric stenosis is most frequently diagnosed in infants between 2-6 weeks of life. Early use of erythromycin has been found to be associated with a higher incidence of pyloric stenosis1.

References
1. Hay WW Jr., Levin MJ, Deterding RR, Abzug MJ. Current Diagnosis & Treatment, Pediatrics. 22nd ed. Lange Medical Publications; 2014: 658-659.
2. Costanzo CM, MD, Vinocur C, MD, Berman L, MD. Prematurity Affects Age of Presentation of Pyloric Stenosis. Clinical Pediatrics. Vol 56, Issue2, pp 127-131. May 4, 2016.
3. Subramaniam S, MD. Pediatric Pyloric Stenosis. Medscape. Nov 20, 2016, Accessed Jun 27, 2017.
4. Mayo Clinic Staff. Pyloric Stenosis. MayoClinic.org. Nov 24, 2015. Accessed Jun 27, 2017.

Answer is C. Shoulder impingement syndrome is a common diagnosis in the orthopedic and primary care setting. The patient population that is most at risk for developing shoulder impingement syndrome is those who reach at the level or above the level of their shoulder for either work or sports on a constant basis (1). Increasing age can also cause osteoarthritic changes and therefore can be another cause of shoulder impingement syndrome. Shoulder impingement syndrome, otherwise referred to as SIS, is not due to a direct injury itself but a compilation of shoulder symptoms (1). SIS is the compression of the anatomical structures within the shoulder joint (1). The shoulder joint is comprised of the rotator cuff muscles (supraspinatus, infraspinatus, teres minor, subscapularis), the subacromial bursa, labrum, and long head of the biceps (1). These structures are located between the humeral head and under the acromion. SIS can occur from a high riding humeral head due to a rotator cuff tear and/or humeral instability, the make up of the acromion, for example numerous osteophytes and/or AC joint arthritis (1). Lastly, SIS can be caused by reduced space between the acromion and humeral head (1). The acromion plays a large role in the development of impingement syndrome. When reviewing a patient’s x-rays it is important to look at the morphology of the acromion. The acromion can be separated into 3 types; Type 1 (Flat), Type 2 (Curved), and Type 3 (Hooked) (1). The increase in type is associated with a decrease in space between the acromion and humeral head (1). This correlates an increase in severity of impingement and increased potential for a rotator cuff tear.
A patient with shoulder impingement will present in clinic typically with a chief complaint of shoulder pain that is worse with overhead activity. The patient may point directly to the AC joint and/or subacromial space as the point of greatest discomfort and they may report radiation to their deltoid or lateral arm (1). During physical exam, patients typically have pain with range of motion. A patient may express discomfort at 30-40 degrees of abduction and at approximately 90 degrees of flexion (1,2). The patient will have minimal difficulty and pain with external rotation however they are characteristically unable to internally rotate due to pain (2). The patient will not have a decrease in strength. Special tests should be performed during exam. A patient with shoulder impingement syndrome will typically have a positive Hawkins test and Neer test which indicates supraspinatus impingement (2). A positive crossbody test indicates AC joint impingement.
Once the diagnosis of shoulder impingement is made either clinically and/ or with x-rays, the management is typically conservative. Further testing, such as a MRI is not clinically indicated unless there is a question of a rotator cuff tear (3). Initial treatment includes rest, ice, NSAIDs, pendulum exercises, and strengthening of the rotator cuff with physical therapy (1,2). If initial management fails it is recommended to try a cortisone injection in the AC joint and/or subacromial space (1, 2). Lastly, if a patient fails conservative management it is recommended to undergo surgical treatment, which is subacromial decompression with or without distal clavicle resection.
Patient’s presenting with a rotator cuff tear will have a decrease in strength in the rotator cuff muscles up on exam and severe tears will have a positive drop arm test (2). The Hawkins, Neer, and Crossbody test may be positive or negative, however the key difference is muscle strength when forming a differential diagnosis between the two. Adhesive capsulitis, also known as frozen shoulder, can be ruled out due this patient’s ability to actively and passively move their shoulder. Patients with adhesive capsulitis will deny pain at rest however they have significant pain with range of motion (2). Due to inflammation and scar tissue adhesions the patient’s range of motion will be limited in all planes (2). A patient with biceps tendinois will also complain of pain with overhead motion however when asked to point to location of pain they will point anterior to the humerus in the intertubercular groove (2). The patient has a short head and long head of the biceps, which when inflamed will cause pain (2). Upon exam patients will have tenderness to palpation of that area and will have pain with resisted supination (2). Biceps tendinosis exam results in a positive Speed’s test and Yergason’s test.

References:

1. Simons SM, Kruse D, Dixon JB. Shoulder Impingement Syndrome. UpToDate. March 2016. https://www.uptodate.com. Accessed July 5, 2017.
2. Rempel DM, Amirtharajah M, Descatha A. Rempel D.M., Amirtharajah M, Descatha A Rempel, David M., et al.Shoulder, Elbow, & Hand Injuries. In: LaDou J, Harrison RJ. LaDou J, Harrison R.J. Eds. Joseph LaDou, and Robert J. Harrison.eds. CURRENT Diagnosis & Treatment: Occupational & Environmental Medicine, 5e New York, NY: McGraw-Hill; 2013.http://accessmedicine.mhmedical.com/content.aspx?bookid=1186&sectionid=6647855. Accessed July 06, 2017.
3. Watts AR, Williams B, Kim SW, Bramwell DC, Krishnan J. Shoulder impingement syndrome: a systematic review of clinical trial participant selection criteria. Shoulder & Elbow. 2016;9(1):31-41. doi:10.1177/1758573216663201.

Answer: (b) – The dashboard mechanism of injury, posterior pain, and positive posterior drawer test indicate that the patient’s PCL is torn. (a) – Incorrect. This is not the best choice because there is no joint line tenderness and no other indications of meniscal tear such as complaints of joint locking and giving way. (c) – Incorrect. Patient is able to perform a straight leg raise. This rules out the possibility of a patella tendon rupture. (d) – Incorrect. A negative anterior drawer test and negative Lachman test rule out disruption of the ACL.
Discussion:
The posterior cruciate ligament is one of four ligaments that stabilize the knee by connecting the femur to the tibia1. The PCL is found inside the knee joint, originating at the posterior tibial sulcus below the articular surface and inserting anterolateral medial femoral condyle2. The PCL functions to minimize posterior translation of the tibia, thus protecting and stabilizing the knee joint1,2. The PCL also protects the knee joint from hyperextension, and stabilizes the knee joint during rotational movements3. Injury of the posterior cruciate ligament makes up only 5-20% of all knee ligamentous injuries2, and often occurs in conjunction with injuries to other structures of the knee such as ligament, cartilage, and bone1. The PCL is significantly stronger than the ACL and is therefore less likely to get injured, and also more difficult to assess for minor injuries. Injury to the PCL is classified as a sprain and there are 3 grades. A Grade 1 sprain indicates the ligament has been slightly stretched, but not compromised to the point where it can no longer stabilize the knee. A Grade 2 sprain, also known as a partial tear, indicates the ligament has become loose. A Grade 3 sprain is a full tear, or rupture, of the ligament and the knee joint is no longer stable1. Most often PCL injuries are partial tears and minimal intervention is needed.
Injury to the PCL is most frequently sustained by a forceful direct blow to the anterior tibia while the knee is in a flexed position; often referred to as a “dashboard injury”1,2,3. The injury can also occur from forced hyperextension of the leg1,2. These injuries are commonly seen in car accidents when a person strikes his lower leg on the dashboard of the car, a tackle injury in contact sports, and from a fall forward onto a flexed knee3. It is less likely to see injuries to the PCL occur from normal activities of daily life, which are often causes of other knee soft tissue injuries.
Excessive posterior translation of the tibia from the force sustained during the previously mentioned injuries exceeds the stabilizing capability of the PCL, 2500-3000N2, and results in injury, or sprain to the ligament1. Extent of PCL sprain is directly related to the amount of posterior subluxation of tibia with the knee at 90 flexion. A Grade 1 sprain has 1-5mm posterior translation, a grade 2 has 6-10mm posterior translation, and a grade 3 has >10mm posterior translation2.
History obtained from the patient with suspicion of PCL injury will include some moment of trauma, whether it be the car accident, tackle, or fall with hyperextension. Symptoms associated with the injury include persistent pain and swelling immediately after injury, difficulty walking, feelings of knee instability, giving way of knee joint especially when walking downhill or descending stairs, and posterior knee pain1,2. However, these symptoms are often subtle or not noticed in isolated PCL injuries2.
The most accurate physical exam test to diagnose a PCL injury is the posterior drawer test performed at 90 flexion. A posterior directed force applied to the proximal tibia will results in >10-15mm posterior translation of tibia in PCL injury2. Laxity at 0 flexion with varus and valgus stress to the knee can also be indicative of PCL injury. The posterior sag sign on physical exam suggest PCL injury. A posterior shift of the tibia of the involved knee is observed when a patient lies on back and flexes both knees to 902.
First line imaging for complaints of knee pain are plan films. AP, supine lateral, and lateral stress views of the affected knee are all appropriate x-rays to order. While x-ray will not show injury to the PCL, they may show avulsion fractures due to acute rupture of the ligament1,2. The lateral stress view is becoming a more popular and frequently used tool in diagnosing PCL injury. The x-ray is taken with the knee flexed to 70 and stress applied to the anterior tibia. Asymmetric posterior tibial displacement of the two knees indicated PCL injury2.
The confirmatory test for diagnosing PCL injury is an MRI of the affected knee. Normally the PCL appears as an uninterrupted dark band on MRI. If there has been injury to the ligament there will be disruption of this dark band evident on MRI3.
There are both surgical and nonsurgical treatments for PCL injuries depending on the patient’s symptoms and degree of injury to the PCL and entire knee joint. Grade 1 and 2 sprains of the PCL are often treated nonsurgically. This treatment includes bracing for protected weightbearing and physical therapy for strengthening of the quadriceps. Patients are able to return to normal activity including sports in 2-4 weeks with successful conservative treatment1,2. In isolated grade 3 sprains in patients who are not athletes, nonsurgical treatment can also be used and includes immobilization in extension for 4 weeks followed by daily range of motion exercises and strengthening2.
In combined ligamentous injuries with knee instability and isolated grade 2 or 3 PCL sprain with avulsion fracture, surgery is indicated to stabilize the knee joint. Because a torn PCL cannot be repaired, reconstruction of the ligament in the surgery of choice. Graft options for PCL reconstruction include autografts, allografts, and artificial material3. Allograft reconstruction is the most frequently used method of reconstruction and tissues include Achilles tendon, bone-patellar tendon-bone, hamstring, and anterior tibialis tendon3. Reconstruction surgery is often performed arthroscopically unless a large avulsion fracture needs repair, in which case an open approach is taken and the bone-tendon-bone graft is inlaid2,3. In the arthroscopic approach, a canal is drilled through the tibia starting on the anterolateral aspect, passing through the insertion point of the PCL and out the medial aspect of the femur. The graft is secured to the tibia with a screw, and held in place on the femur using a stabilizing button2,3. Post surgically patients are immobilized in extension. Physical therapy begins 1-4 weeks post surgery, and full recovery and return to normal activity requires between 6 and 12 months1,2,3. Surgical techniques for PCL reconstruction continue to improve, and generally patients have good success and full recovery.
REFERENCES:
1. Posterior Cruciate Ligament Injuries.” Posterior Cruciate Ligament Injuries-OrthoInfo – AAOS. American Orthopedic Society for Sports Medicine, 01 Feb. 2009. Web. 08 July 2017.
2. Allen, Deborah, MD. “PCL Injury.” Orthobullets. Lineage Medical, 2011. Web. 08 July 2017.
3. Orthopaedic Procedures | Posterior Cruciate Ligament Reconstruction.” One Health. The One Health Group, n.d. Web. 08 July 2017.

Correct answer: (D) postpartum psychosis or brief psychotic disorder with peripartum onset. This patient is experiencing delusional thoughts of guilt or sin, paranoia, thought-blocking and appears internally preoccupied. Risk factors seen here for PP include parturition within one month and degraded sleep pattern. Collateral information from family and friends is oftentimes essential, and based on the husband’s report of hyper-verbal behavior it is possible that this is an initial presentation of (E), bipolar disorder with mania, however more time and outpatient treatment will be necessary to clench such a diagnosis. The patient may have elements of an obsessive-compulsive disorder (A) because of her fixated concern about caring for the infant, however would not be a leading diagnosis in this case at this time. There is no information in this scenario regarding the patient’s past history of a depressive disorder (B), and while it is normal for a new mother to lack sleep and feel concerned for the infant, the delusional thoughts and overprotectiveness are not a normal postpartum response (C).

PP is a medical emergency due to the high risk of suicide and infanticide. Other risk factors include family history of postpartum depression or bipolar disorder, endocrine dysregulation, infection and sleep disturbances. Symptoms may include: delusions or hallucinations, irritability, hyperactivity, paranoia, rapid mood swings and difficulty concentrating.

Discussion: Postpartum Psychosis
Epidemiology
Prevalence is 1-2 occurrences per 1,000 births. In females, a higher risk of psychosis is noted during the first few weeks, most notably between days 3-10 following birth than at any other time. A family history of mental illness, postpartum depression or psychosis increases the risk. For women with known psychiatric illnesses, the postnatal period is a period of high relapse. 1This is a medical emergency due to the increased risk of suicide and infanticide.
Etiology: Postpartum psychosis is precipitated by childbirth, with a significant increase in risk for first time mothers. It is thought that it is due to physiological changes surrounding childbirth combined with genetic predisposition that are likely at play. Additionally, there may be endocrine, hormonal, immunological, circadian rhythm changes that contribute to the risk for PP; life events and psychosocial stressors are not considered to be triggers. 2
A consideration in the onset of postpartum psychosis is that it may be a first break psychosis with mania in bipolar disorder that coincides with hormonal shifts after delivery. PP is a possible onset or recurrence of primary psychotic disorder such as schizophrenia. 1
Presentation: Normally, PP presents in the postnatal period within the first month. It is often severe, with prominent confusion and fluctuating symptoms as mixed affective, schizoaffective, or manic states. 1
Symptoms may include: Delusions or strange beliefs, Hallucinations (seeing or hearing things that aren’t there), Feeling very irritated, Hyperactivity, Decreased need for or inability to sleep, Paranoia and suspiciousness, Rapid mood swings, Difficulty communicating at times.
Differential Diagnosis: Depressive episode with psychotic features, Schizophrenia, Mania or mixed episodes features, Obsessive compulsive disorder, Alcohol or substance withdrawal, Anti-NMDAR encephalitis, Delirium or psychosis due to including acute infection, peripartum blood loss and anemia, and exacerbation of predicting endocrine and/or autoimmune disease.

Treatment
Relatively little is known in the prevention and treatment, although investigations in the use of ECT, antipsychotics, mood stabilizers, hormones, and the beta-blocker propranolol have been documented.
The treatment of postpartum psychosis ideally entails medical management with neuroleptic agents, mood stabilizers or antipsychotics. Often, inpatient psychiatric setting is warranted, and social services must be recruited and consideration given to electroconvulsive therapy (ECT) in refractory cases. The separation of mother and infant is important until the resolution of all symptoms of psychosis. Counseling services should be recruited once patient’s disorganized thought processes have been minimized, and the patient should be educated regarding their symptoms and possible recurrences, treatment and outcomes. 2
Medications
Postpartum psychosis is treated in the same fashion as other psychotic disorders. It is important that breastfeeding is be taken into consideration, and that the patient make an informed decision whether to continue nursing the infant. Psychotropic medications are not absolute contraindications in breastfeeding, however the infant must be monitored for sedation or extrapyramidal symptoms (EPS). EPS may include muscle spasms or contractions, akathisia (motor restlessness), parkinsonism (rigidity, bradykinesia, tremor), tardive dyskinesia (irregular, jerky movements). Aim for monotherapy.

Monitor
Note any exacerbation in symptoms
Mental status to include thought content, though process, affect, and mood
Endocrine and/or thyroid function
Infection recurrence
Side effects to medications

Patient Counseling
Rest or sleep when your baby sleeps. The housework will wait
Seek out practical help in the house – friends, family or a volunteer
Take short walks in the daytime
Share responsibility for night feeds if you possibly can
Talk to your Mental Health Team about how you are feeling. Taking medication at bedtime might reduce sleepiness in the day.

References
1. DynaMed Plus. Postpartum psychosis. http://www.dynamed.com/topics/dmp~AN~T116521/Postpartum-psychosis. Published 1995. Updated 2016 Sep 05 12:00 AM (ET). Accessed July 9, 2017, 2017.
2. Bergink V, Rasgon N, Wisner KL. Postpartum psychosis: Madness, mania, and melancholia in motherhood. Am J Psychiatry. 2016;173(12):1179-1188. https://ezproxymcp.flo.org/login?url=http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=psyc13&AN=2017-04781-007; http://resolver.ebscohost.com/openurl?sid=OVID:psycdb&id=pmid:&id=doi:10.1176%2Fappi.ajp.2016.16040454&issn=0002-953X&isbn=&volume=173&issue=12&spage=1179&date=2016&title=The+American+Journal+of+Psychiatry&atitle=Postpartum+psychosis%3A+Madness%2C+mania%2C+and+melancholia+in+motherhood.&aulast=Bergink.
3. Doucet S, Jones I, Letourneau N, Dennis C, Blackmore ER. Interventions for the prevention and treatment of postpartum psychosis: A systematic review. Archives of Women’s Mental Health. 2011;14(2):89-98. https://ezproxymcp.flo.org/login?url=http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=psyc8&AN=2011-08555-001; http://resolver.ebscohost.com/openurl?sid=OVID:psycdb&id=pmid:&id=doi:10.1007%2Fs00737-010-0199-6&issn=1434-1816&isbn=&volume=14&issue=2&spage=89&date=2011&title=Archives+of+Women%27s+Mental+Health&atitle=Interventions+for+the+prevention+and+treatment+of+postpartum+psychosis%3A+A+systematic+review.&aulast=Doucet.
4. Action on Postpartum Psychosis. Insider guide – recovery after postpartum psychosis. 2013.

Correct answer: D. tinea manuum
The correct answer here is D. tinea manuum, a tinea infection of the hand(s). Tinea infections can occur in any age and are almost always pruritic. Tinea manuum presents similarly to tinea corporis except it is located on the hand as opposed to the other parts of the body. Tinea manuum most commonly occurs unilaterally and annular. Most dermatophyte infections are erythematous with scaling involved.1 A common cause of tinea is contact with animals as well as soil.2 This patient admitted to working on his friend’s farm. Answer A. contact dermatitis could be considered with a rash on the hands due to most patients not realizing when they encounter an irritating substance. However, the patient does not recall using anything new and the rash is unilateral. Contact dermatitis also has a lower incidence in males.3 Answer B. psoriasis, has a variant that can occur on the hands. This is called pustular psoriasis and does not fit the description of the rash. The rash does not involved pustules which is the primary lesion in this type of psoriasis. The patient is also only 25 years of age and the most common age to be diagnosed with psoriasis is between 40-60.4 Answer C. dyshidrotic eczema can be considered because it leaves the hands scaly and itchy. It can also be erythematous although it does not present in an annular shape. Dyshidrotic eczema is almost always bilateral and is usually caused by sweating or excessive moisture on the hands.5 This seems unlikely with the patient’s job description. It is extremely pruritic and most commonly presents with vesicles.

References
1. Goldstein A, Goldstein B. Dermatophyte (tinea) infections. UpToDate. https://www.uptodate.com/contents/dermatophyte-tinea-infections?source=search_result&search=tinea manuum&selectedTitle=1~9. Published 2017. Accessed July 11, 2017.

2. Hainer BL. Dermatophyte Infections. American Family Physician. http://www.aafp.org/afp/2003/0101/p101.html. Published January 1, 2003. Accessed July 11, 2017.

3. Goldner R, Tuchinda P. Irritant Contact Dermatitis in Adults. Up. https://www.uptodate.com/contents/irritant-contact-dermatitis-in-adults?source=search_result&search=contact dermatitis&selectedTitle=1~150. Published 2017. Accessed July 11, 2017.

4. Kalb R. Pustular psoriasis: pathogenesis, clinical manifestations, and diagnosis. UpToDate. https://www.uptodate.com/contents/pustular-psoriasis-pathogenesis-clinical-manifestations-and-diagnosis?source=search_result&search=psoriasis&selectedTitle=3~150. Published 2017. Accessed July 11, 2017.

5. Adams D, Marks Jr. J. Acute palmoplantar eczema (dyshidrotic eczema). UpToDate. https://www.uptodate.com/contents/acute-palmoplantar-eczema-dyshidrotic-eczema?source=search_result&search=dyshidrotic eczema&selectedTitle=1~23. Published 2017. Accessed July 11, 2017.

Infective endocarditis (IE) was recognized as a complication of IVDU in the 1950s. It is estimated to occur at a rate of 2-4 cases per 1000 years of IVDU.1 Infective endocarditis occurs when bacteria stick to the inside of the heart and valves and replicate. There are many predisposing factors that increase the risk of IE. Injectable synthetic material causes direct damage to the endothelial tissue, drugs such as heroin may cause direct toxic damage to the valves themselves, users may inject organisms from their skin because of improper skin cleansing, and use of saliva as a diluent leads to an increased risk of infection with oropharyngeal flora.1 The most common organism isolated from IVDU associated IE is Staphylococcus aureus. Assessment of a patient with acute IE may sometimes be challenging. They usually present with an acute septic picture. Physical exam findings can include, but not be limited to; fever, weakness, signs of heart failure, a heart murmur, peripheral septic emboli leading to splinter hemorrhages, janeway lesions, conjunctival hemorrhages, or other end-organ damage. End-organ damage can manifest in bone pain, acute kidney injury with or without hematuria, altered mental status or a change in sensorium due to brain emboli, and rashes or lesions on the skin due to septic occlusion of the distal capillaries.1 Diagnosis of IE can be made using the Duke Criteria. The diagnostic tests that need to be done for the Duke Criteria are blood cultures and an echocardiogram. The other components of the diagnostic criteria are a fever >100.4*F, immunologic phenomena (glomerulonephritis, osler nodes, roth spots), vascular phenomena (arterial emboli, pulmonary infarct, janeway lesions, intracranial bleed, conjunctival hemorrhages), and predisposing conditions like IVDU can all be made clinically.2 Management of IE is antibiotic therapy dependent on the susceptibility profile of the organism isolated in blood cultures. Blood cultures may take a few days to come back so broad-spectrum antibiotics to cover gram-positive organisms including MRSA should be initiated as soon as a presumptive diagnosis is made. If valve or heart wall involvement is extensive or an abscess is formed, valve replacement therapy and tissue debridement may need to be used in the treatment process. In cases of the IE with Staphylococcus aureus, treatment should be for 4-6 weeks.3

Explanation:
Blood cultures are an option for all 4 choices provided. In suspected IE it is one of the first tests that should be ordered before broad-spectrum antibiotics are initiated. Blood cultures are important because it allows us to isolate an organism and find its susceptibility profile. Duration of treatment for IE is dependent on organism isolated. According to the Infectious Disease Society of America, Strep spp. can be treated for 4 weeks, while Staph spp. should be treated for 4-6 weeks.3 The next part of the question asks about imaging modalities. The main concept behind this question is that it is important to differentiate between sepsis and IE with potential vegetation in the heart or the heart valves. The treatment times for sepsis can range from 2-4 weeks while the treatment time for IE will be a minimum of 4 weeks. A chest x-ray will not provide us with any clues as to whether or not there is vegetation on one of the heart valves. An abdominal ultrasound would not be used in this scenario because it would provide little diagnostic utility for our patient’s condition. A trans-thoracic echo could potentially be done, but a trans-esophageal echo provides better visualization of the areas of the heart that could be affected, including the heart valves. A trans-esophageal echo has a high sensitivity for picking up heart valve vegetation than a trans-thoracic echo.4 The correct answer is B, blood cultures and a trans-esophageal echo should be performed to determine the duration of antibiotic treatment.

References
1. Sexton, MD D, Chu, MD, MHS V. Infective endocarditis in injection drug users. Uptodatecom. 2017. Available at: https://www.uptodate.com/contents/infective-endocarditis-in-injection-drug-users?source=search_result&search=ivdu%20endocarditis&selectedTitle=1~150#H6. Accessed July 5, 2017.
2. Endocarditis Diagnostic Criteria (Duke Criteria). Referencemedscapecom. 2017. Available at: http://reference.medscape.com/calculator/endocarditis-diagnostic-criteria-duke. Accessed July 5, 2017.
3. Baddour L. Infective Endocarditis: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Statement for Healthcare Professionals From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: Endorsed by the Infectious Diseases Society of America. Circulation. 2005;111(23):e394-e434. doi:10.1161/circulationaha.105.165564.
4. Evangelista A. Echocardiography in infective endocarditis. Heart. 2004;90(6):614-617. doi:10.1136/hrt.2003.029868.